The lytic growth of bacterial and animal viruses, production of colicins, cell division in prokaryotes and oncogenesis are all induced by the same class of agents, i.e., radiation, mitomycin, thymineless death, chemicals which affect DNA synthesis and repair, etc., and may operate through common molecular mechanisms. The writer has proposed a mechanism of lambda-virus induction which may have widespread applicability to other inducible systems mentioned above. The lambda repressor is assumed to have affinity not only for lambda operators, but also for single strand lesions when present in the host DNA. All of the agents listed are known to produce such lesions and according to the model, induction, i.e., derepression would occur when the capacity of the cell to repair the lesions is exceeded. Significant evidence supporting this model was provided by in vitro binding studies in which purified DNA from treated E. coli competed with lambda DNA for binding with lambda repressor present in crude extracts. Recent experiments have shown that single strand gaps in double stranded E. coli DNA compete much better than nicks. The writer now proposes (1) to extend these studies with purified lambda ind positive and lambda ind negative repressor and determine association and dissociation constants to well defined DNA lesions and other non-operator DNAs; (2) to find out the nature of the repressor-non-operator association; (3) to study the in vivo formation of single strand gaps during post-irradiation incubation; (4) to test the applicability of the model to other inducible systems in prokaryotes and eukaryotes. This study will help elucidate the genetic control of episomes at the molecular level. If the model can be shown to be applicable to cancer induction by tumorigenic agents, it could shed considerable light on oncogenesis and thus be important for health-related activities.